Intro to Counterstrain Flashcards
What is counterstrain?
dysfunction which inhibited by apply a position of mild strain in direction exactly opposite to that of the false strain effect
use specific point of tenderness related to this dysfunction followed by specific directed positioning to achieve the desire
Posterior Tender points
PT3-5
PT6-UPL5
What invented counterstrain?
Lawrence Jones DO
1955
discovered posterior tender points
Trigger point vs Tender point
Trigger point
- pt present with characteristic pain pattern
- located in muscle tissue
- locally tender
- elicits jump sign and radiating pain pattern
- taut band of tissue
- twitch response with snapping palpation
- demographia of skin over point
Tender point
- no pain pattern
- located in muscles, tendons, ligaments, fascia,
- locally tender
- jump sign but NO radiating patterin
- taut band not present
- twitch response not present
- demographia
Treatment for trigger point and tender point
Trigger point
- spray and stretch
- trigger point injection
Tender point
- spontaneous release by positioning (counterstrain)
Trauma Physiology
trauma
1) changes in myofascial tissue at microscopic and biochemical leve
2) damage to myofibrils and microcirculation
Nociceptive information to CNS
Counterstrain Theories
1) Nociceptive model
2) proprioceptive model
3) four phases of counterstrain
Nociceptive Model
- mechanism of action
- example (ankle sprain)
a tissue is strained recruiting nociceptors within that tissue (muscle, tendon, ligament)
Reflexive contraction of affected tissues
contraction of affected tissue become neutral
Ankle
- reflexive contraction occurs at lateral ankle
- contraction of the lateral ankle becomes the new neutral
Proprioception Model
- mechanism of action
- example- whip lash
maintain tone for a period after the stimulus has ended
Muscle spindle fiber
- excessively rapid stretch of primary spindle cell can induce a protective contraction in extrafusal fibers related to it, which can maintain tone for a period after the stimulus has ended
Muscle is strained (agonist)-> antagonist muscle is shortened ( turns down spindling fire rate) => CNS turns up gain for antagonist gamma system
-> antagonist contraction become “neutral”
Whiplash
- posterior cervical muscles are strained
- anterior cervical muscles shorteneed CNS turns up gain for antagonist gamma system
- antagonist contraction becomes the new neutral
Counterstrain Theory: Nociceptor
- nociceptor recruitment
- agonist (affected tissue) shortened
- agonist tissue shortening
Counterstrain Theory:
proprioceptor
antagonist muscle shortened
antagonist muscle shortening becomes new neutral
gamma loop becomes new neutral
nociceptor vs proprioceptor models
local constriction of muscles causes decreased circulation, causing localized edema and back up products of metabolism
Phases of counterstrain
1) relaxation
2) reset of spindle fibers and nociceptors
3) washout
4) slow return to neutral
Phase of Counterstrain: relaxation
shortened the affected tissue in 3 planes
- flexion/extension
- sidebending
- rotation
- sometimes traction or compression
rapid reduction in noiceptive input
Phase of Counterstrain: spindle reset
primary endings of muscle spindle stretch receptors (annulospiral)
- length
- rate of change in length of muscle (dynamic)
secondary endings of muscle spindle stretch receptors ( flower spray)
- length
- not dynamic changes (static)